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Originally published In Press as doi:10.1074/jbc.C200450200 on September 2, 2002

J. Biol. Chem., Vol. 277, Issue 43, 40181-40184, October 25, 2002
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ACCELERATED PUBLICATION
Biological Evidence That SOCS-2 Can Act Either as an Enhancer or Suppressor of Growth Hormone Signaling*

Christopher J. GreenhalghDagger §, Donald MetcalfDagger , Anne L. ThausDagger , Jason E. CorbinDagger , Rachel UrenDagger , Phillip O. MorganDagger , Louis J. Fabri, Jian-Guo ZhangDagger , Helene M. MartinDagger , Tracy A. WillsonDagger , Nils Billestrup||, Nicos A. NicolaDagger , Manuel BacaDagger , Warren S. AlexanderDagger , and Douglas J. HiltonDagger

From Dagger  The Walter and Eliza Hall Institute of Medical Research and the Cooperative Research for Cellular Growth Factors, PO Royal Melbourne Hospital, VIC 3050, Australia,  AMRAD Operations Ltd., Richmond 3121, Australia, and the || Steno Diabetes Center, Niels Steensens Vej 2, DK-2820 Gentofte, Denmark

Suppressor of cytokine signaling (SOCS)-2 is a member of a family of intracellular proteins implicated in the negative regulation of cytokine signaling. The generation of SOCS-2-deficient mice, which grow to one and a half times the size of their wild-type littermates, suggests that SOCS-2 may attenuate growth hormone (GH) signaling. In vitro studies indicate that, while SOCS-2 can inhibit GH action at low concentrations, at higher concentrations it may potentiate signaling. To determine whether a similar enhancement of signaling is observed in vivo or alternatively whether increased SOCS-2 levels repress growth in vivo, we generated and analyzed transgenic mice that overexpress SOCS-2 from a human ubiquitin C promoter. These mice are not growth-deficient and are, in fact, significantly larger than wild-type mice. The overexpressed SOCS-2 was found to bind to endogenous GH receptors in a number of mouse organs, while phosphopeptide binding studies with recombinant SOCS-2 defined phosphorylated tyrosine 595 on the GH receptor as the site of interaction. Together, the data implicate SOCS-2 as having dual effects on GH signaling in vivo.

* This work was supported by the Anti-Cancer Council of Victoria, Melbourne, Australia; AMRAD Operations Pty. Ltd., Melbourne, Australia; the National Health and Medical Research Council, Canberra, Australia; the J. D. and L. Harris Trust; National Institutes of Health Grant CA-22556; and by the Australian Federal Government Cooperative Research Centers Program.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ Supported by an Australian Postdoctoral Research Fellowship from the Australian Research Council. To whom correspondence should be addressed. Tel.: 61-3-9208-4021; Fax: 61-3-9208-4100; E-mail: greenhalgh@wehi.edu.au.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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